Abstract
1. In order to increase our understanding of the central regulation of human cardiac vagal motoneurones we studied the interaction between two opposing influences on cardiac vagal tone, one related to diving and the other to exercise. 2. The heart rate response to cooling the face (0 degrees C, trigeminal cutaneous receptor stimulation, TGS) and to a brief isometric muscle contraction was studied in fourteen healthy young adults (8 males, 6 females) during controlled ventilation at supine rest. 3. Fluctuations in R-R interval were quantified by spectral analysis. In addition the absolute values of R-R intervals occurring in any one of ten arbitrary phases of a respiratory cycle were measured over thirty to sixty cycles to give a graph of the changes in R-R interval throughout a respiratory cycle. 4. TGS produced a significant decrease in heart rate (-21 +/- 2 beats min-1 in females, -19 +/- 2 beats min-1 in males; means +/- S.E.M.). In addition the autospectral plots of R-R interval variability showed that during TGS there was a significant increase both in the high frequency peak and in the low frequency peak in all subjects. These data suggested that in these experiments the bradycardia of TGS was due to an increase in cardiac vagal tone. 5. Voluntary isometric contractions at 40 and 60% of maximum (40% MVC, 60% MVC) were timed to occur early in expiration or early in inspiration. Analysis of the changes in R-R interval produced by these contractions was confined to the respiratory cycle in which they were initiated. The early onset of these changes was interpreted as showing a decrease in cardiac vagal tone. 6. The 40% MVC and 60% MVC increased heart rate significantly within one respiratory cycle with maximum effects having a mean of 9.5 +/- 3 and 11 +/- 3 beats min-1, respectively. When isometric muscle contraction was initiated during TGS the 60% MVC but not the 40% MVC was able to significantly decrease R-R interval and hence increase heart rate. 7. It is concluded that the TGS excitatory inputs and the muscle inhibitory inputs to cardiac vagal neurones do not interact by one input gating the other early in the pathway but more probably by a process of algebraic summation closer to the cardiac vagal neurone.